Heart disease is responsible for one out of every four deaths in the United States, making it the number one killer in our nation (Parker, Health Guidance, 2012). Survivors of myocardial infarctions (heart attacks) are left with scar tissue that cannot function like that of healthy myocardial muscle, leading to limitations on physical activity and exertion. By developing this scar tissue, the human body considers the heart healed, but the heart remains damaged due to its inability to function as successfully as before the myocardial infarction. On average, 600,000 people suffer from heart attacks in the United States yearly with 190,000 of those cases happening to people who have already experienced a heart attack (CDC, 2013).
Cardiogenesis and its related pathways are very significant for the treatment and prevention of heart disease. The Mexican axolotl, Ambystoma mexicanum, is a vertebrate animal model for studying myofibrillogenesis due to its naturally-occurring lethal recessive mutation caused by gene c for “cardiac non-function”. Homozygous recessive (c/c) “mutant” embryos have hearts consisting of only a single layer of cells and lacking organized myofibrils. The mutant hearts fail to beat. Among some earlier studies, it was discovered that the necessary components of the sarcomere did not become organized into functioning myofibrils in mutant organisms and the reason that they did not conjugate correctly was due to an absence of muscle tropomyosin (Lemanski, Dev. Biol., 1973, and Zhang, J. of Cellular Biochem., 2007).